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Clin Med III - GI > Hernias, Biliary dz, Hepatitis > Flashcards

Hernias, Biliary dz, Hepatitis Flashcards

1
Q

define hernia & name the types of hernias

A

protrusion, bulge, or projection of any organ or part of an organ through the body wall that contains it

  • Groin Hernias - Inguinal-most common-80% (Indirect and Direct)
  • Femoral- 10%
  • Other
  • Umbilical, incisional, etc
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2
Q

si/sx of a hernia

A

Lump

  • Often worse at the end of the day
  • May resolve with lying flat

Abdominal fullness/discomfort

Pain with lifting or exertion

Constipation

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3
Q

Conservative Tx for hernias

A

Conservative Who:

  • Men: may use conservative treatment if small, reducible, minor discomfort
  • Women: Not recommended to treat conservatively- go right to surgical repair
  • Recurrent: not recommended

Conservative How:

  • Heat and self reduction with lying flat
  • Trusses and hernia belts - Associated problems
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4
Q

indications for urgent surgicla repair of hernias

A

Surgery Urgent surgical repair

  • For incarcerated or causing bowel obstruction
  • Pain, fever, sometimes erythema, nausea, vomiting, signs of bowel obstruction
  • Goal is within 6 hours of onset of incarceration
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5
Q

dx hernias

A

Good clinical exam

  • Use gloved finger into the scrotum and into the inguinal ring, ask patient to bear down and check for a palpable bulge
  • Palpate groin and femoral area for lumps

Imaging if bad exam”

Start with ultrasound and then use MRI if suspicion still exists because MRI is more sensitive and specific (Herniography

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6
Q

define loactions fo hernias

Indirect(most common)

Direct

Femoral

A

Indirect(most common)

  • Follows spermatic cord into the scrotum
  • Lateral to the inferior epigastric artery
  • Originates in the deep inguinal ring and passes through the superficial inguinal ring

Direct

  • Bulges through abdominal wall in area of weakness in inguinal canal
  • Medial to inferior epigastric artery
  • Only passes through the superficial inguinal ring

Femoral

  • Bulges through abdominal wall
  • Inferior to the Inguinal ligament
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7
Q

women are most likely to get what kind of herna

A

femoral

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8
Q

describe progression of pilonidial dz

A
  1. Starts as a small non-painful area in the skin above the coccyx/upper half of gluteal cleft called a Pilonidal sinus
  2. Fills up with pus and debris and develops a tract to the surface called a Pilonidal cyst
  3. Painful, red, swelling
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9
Q

what is most common cause of rectal bleeding

A

Hemorrhoids

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10
Q

decribe the 2 classifications of hemhorroids

A

Internal Hemorrhoids

  • Above the dentate line
  • Classified according to the degree of prolapse
  • Present with painless bleeding
  • Four degrees of classification

External Hemorrhoids

  • Located in the distal third of anal canal
  • Below the dentate line-very painful
  • Can become thrombosed: clot in the hemorrhoid
  • Easy to see on exam
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11
Q

Cardinal Signs of internal hemorrhoids:

A
  • painless bleeding
  • rectal protrusion
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12
Q

name the degrees of internal hemhorroids

A

First Degree -Bulge in lumen of canal on palpation

Second Degree - Protrusion with BM with spontaneous reduction after

Third Degree - Protrude spontaneously or with BM but requires manual reduction

Fourth Degree -Permanently prolapsed and irreducible

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13
Q

Painless Bleeding after defecation-drops into bowl-BRBPR is what degree of hemhorroid

A

first

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14
Q

degree of hemhorroid?

Anal mass with defecation

  • feeling of incomplete evacuation
  • mucus or fecal leakage
A

third

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15
Q

what degree of hemhorroid

Irreducible anal mass

may have painful bleeding

A

fourth

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16
Q

tx of first and second degree hemhoroids

A

Diet

Banding

Sclerotherapy

Infrared coagulation

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17
Q

tx of third and fourth degree hemhorroids

A

Banding

Hemorrhoidectomy

Procedure for Prolapse and Hemorrhoids (PPH)

Transanal Hemorrhoidal dearterialization (THD

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18
Q

hemhorroid tx modality:

Better for immunocompromised and those on anticoagulants

avoid in immunocompromised pts

A

Better for immunocompromised and those on anticoagulants - Sclerotherapy

avoid in immunocompromised pts - rubber band ligation

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19
Q

complication most concerning for tx of hemhorroids

A
  • Concern for incontinence since hemorrhoids provide up to 20% of anal resting pressure
  • Removing them reduces resting pressure and can result in incontinence (what we worry about)
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20
Q

medication options for hemhorroids

A
  • Diltiazem 2% ointment
  • Botox
  • Liposomal bupivacaine
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21
Q

define anal fissures

A

tear in the anoderm distal to the dentate line (PAIN)

Most commonly seen in midline posterior

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22
Q

what are some primary and secondaery causes of anal fissures

A

Primary caused by overstretching of the anal canal

  • Chronic constipation-hard stool
  • Vaginal delivery
  • Anal intercourse

Secondary Causes are the result of another medical cause

  • IBD
  • Previous Anal Surgery
  • Granulomatous Diseases: TB, sarcoidosis
  • Malignancy
  • STDs
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23
Q

differentiate b/w acute and chronic fissures

A

Acute Fissure - Heals within 6 weeks

  • On exam, looks like a small laceration with vascularization
  • Half will go on to become a chronic fissure
  • Treat with conservative management

Chronic Fissure Lasts more than 6 weeks despite conservative management

  • On exam, paler with raised edges
  • Can cause a pile which is also sometimes called a skin tag
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24
Q

conservative tx of anal fissures

A

Stool management

  • Increase fiber (25-30g per day), Decrease fat intake, Increase water intake
  • Stool softener, Sitz Baths

Botox

•Injected into sphincter to help relieve spasm by inhibiting acetylcholine-”chemical sphincterotomy”

more successful in women

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25
Q

name surgical tx for anal fissures and their pros and cons

A

Lateral Internal Sphincterotomy: risk of incontinence

  • Leave open to prevent abscess/infection
  • Success 90%; permanent solution

Endoanal V-Y Advancement Flap: no risk of incontinence

  • Preserves internal and external sphincters
  • May reoccur
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26
Q

If fissure does not heal after 6 weeks…..?

A

consider endoscopy to look for Crohns

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27
Q

causes of anal abscesses

A

Almost all abscesses are caused by infected anal crypt gland

Located along dentate line

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28
Q

what is the Crypto glandular hypothesis;

A

Crypto glandular hypothesis;

states that an infection begins in the anal canal glands and progresses into the muscular wall of the anal sphincters to cause an anorectal abscess

  • Bacteria can get inside the crypt and then spread through the anal duct to the glands
  • Infection spread anywhere from here in the area of “least resistance”
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29
Q

si/sx of anal abcesses

A

Severe pain with sitting

Fever and malaise

Sometimes pain with bowel movements but not always

Purulent Discharge

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30
Q

name deep and superficial anal abcesses

A

Deep

  • Intersphinteric
  • Supralevator

Superficial

  • Subcutaneous/perianal
  • Ischiorectal
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31
Q

dx of anal abcesses

A
  • Lateral decubitus position
  • Redness, fluctuance, induration
  • Digital Rectal Exam
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32
Q

tx of anal abcesses

complications?

A

Incision and Drainage

Antibiotics

Complications

  • Spread of infection
  • Development of fistula

•About half of patients develop anal-rectal fistulas

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33
Q

define anal-rectal fistula

most common type?

A

An abnormal connection between an anal abscess and the rectal canal caused by abscess (cryptoglandular infection)

•Most common is intersphincteric fistula

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34
Q

tx of Anal-Rectal Fistula

A

Seton suture

  • keeps the tract open until it starts to heal
  • If pus stops within 6-8 weeks then can glue or put in a fistula plug

Fistula Plug: Fibrin plug that Helps to heal fistula

Endorectal advancement flap: Extreme cases without healing require surgery

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35
Q

when draining anal-rectal fistula it is important to remember…

A
  • Drain as close to the sphincter as possible
  • Drain supralevator abscess into the rectum
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36
Q

Define

Cholelithiasis

Choledocholithiasis

Biliary colic

A
  • Cholelithiasis: The presence of gallstones.
  • Choledocholithiasis: Gallstones in the bile ducts/common bile duct (CBD)
  • Biliary colic: Intermittent, usually postprandial pain caused by temporary blockage of cystic duct, usually by a gallstone.
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37
Q

define

Cholecystitis (Acute):

chronic

Acalculous cholecystitis

Cholangitis (Acute/Chronic):

A
  • Cholecystitis (Acute): inflammation of the gallbladder, usually caused by build-up of bile when a stone lodges in the neck or cystic duct.
  • Cholecystitis (Chronic): Recurring cholecystitis or mild, chronic inflammation that may be subclinical
  • Acalculous cholecystitis: Inflammation of the gallbladder in the absence of cholelithiasis
  • Cholangitis (Acute/Chronic): Infection/Inflammation of the CBD, usually due to either a gallstone, neoplasm, or stricture
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38
Q

si/sx of Cholelithiasis (Gallstones

A

Severe, intermittent, often post-prandial RUQ pain or epigastric pain – biliary colic

steady pain after eating

radiates to scapula

Patients usually have a history of similar, less severe episodes – be sure to ask about this!

Patient may report intermittent heartburn or reflux, nausea, vomiting, decreased appetite

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39
Q

imaging modality of Cholelithiasis (Gallstones

A

US is primary choice – very sensitive, even for small stones (~2mm)*

•Obese patients - CT scan or MRCP if able to tolerate

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40
Q

tx of Cholelithiasis (Gallstones)

A

Asymptomatic – leave them be

Symptomatic cholelithiasis – refer to general surgery for lap CCY

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41
Q

Risk factors for Cholelithiasis (Gallstones)

A

Risk Factors:

  • Fat –> bariatric surgery or rapid weight loss
  • Female
  • Fertile (pregnancy)
  • 40s
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42
Q

Most common complication of gallstone disease

A

Cholecystitis

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43
Q

Si/Sx of Cholecystitis

A

Biliary colic – post-prandial RUQ/epigastric pain that progressively worsens* - does not go away w/ Pepcid

radiates to scapula

(+) Murphy’s sign (97% sensitive but only 48% in elderly)

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44
Q

physical exam findings in

Cholelithiasis (Gallstones) vs Cholecystitis

A

Cholecystitis (+) murphys sign

Cholelithiasis (Gallstones) - Patients usually have a history of similar, less severe episodes – be sure to ask about this!

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45
Q

US & HIDA findings in Cholecystitis

A

US : may show cholelithiasis, thickened GB wall/pericholecystic fluid. - imaging of choice

HIDA : failure of the gallbladder to fill, usually reserved for after an equivocal US

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46
Q

tx of Cholecystitis

A

symptoms resolve (biliary colic): outpatient surgical referral w/instructions to return to ED if sx return, advise low-fat diet

Persistent Symptoms: Admit or refer for hospital admission and surgical evaluation

OR: Per surgery -> Lap chole (preferably elective) or open if necessary

not a surgical candidate, consider percutaneous cholecystostomy drain via IR

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47
Q

Cholelithiasis (Gallstones) lab findings are usually ??

A

unremarkable

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48
Q

Choledocholithiasis is due to ?

A

Most commonly due to passage of stones from the gallbladder through the cystic duct into the common bile duct

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49
Q

Si/Sx of Choledocholithiasis

A

RUQ pain, jaundice

dark urine

(+) Murphy’s sign

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50
Q

lab values in Choledocholithiasis

A

↑direct bili ( not indirect bilirubin),

↑ AST/ALT

↑alk phos (slow), Lipase

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51
Q

Best non-invasive test for Choledocholithiasis

A

MRCP

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52
Q

tx of Choledocholithiasis

A

ERCP (Endoscopic Retrograde Cholangiopancreatography) -> remove stones

Laparoscopic CCY (typically AFTER ERCP) preferably prior to discharge

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53
Q

Clinical syndrome characterized by fever, jaundice, and abdominal pain that develops as a result of stasis and infection in the biliary tract – usually due to choledocholithiasis

A

Cholangitis

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54
Q

si/sx of cholangitis

A

Charcot’s Triad – Fever, jaundice and RUQ pain( hx of biliary colic)*

Reynold’s Pentad – Fever, Jaundice, RUQ pain, + hypotension and AMS*

Acutely sick – on verge of sepsis

55
Q

pathogens for cholangitis

A

E. coli (25-50%)

Klebsiella (15-20%)

Enterobacter spp.(5-10%)

Enteroccoccus spp. (10-20%)

56
Q

imaging modality for cholangitis

A

ERCP – stone extraction +/- biliary stent placement*

57
Q

tx of cholangitis

A

ADMIT, may need ICU level management

ABCs

Broad-Spect Abx after 2 sets of Blood Cx

  • Zosyn , Ceftriaxone
  • Levaquin with Flagyl IV

Contact GI or Advanced Endoscopy – Patient needs an urgent ERCP with sphincterotomy, stone removal, and biliary drainage (Should be done within 24-48 hours)*

58
Q

Chronic progressive disorder of unknown etiology that is characterized by

inflammation, fibrosis, and stricturing of medium and large ducts in the intrahepatic and/or extrahepatic biliary tree

leads to complications of cholestasis and hepatic failure

A

Primary Sclerosing Cholangitis (PSC)

59
Q

Primary Sclerosing Cholangitis (PSC) is associated w/ what diseases?

A

•Associated with IBD (Ulcerative Colitis)*

60
Q

si/sx of Primary Sclerosing Cholangitis (PSC)

A

Usually Asymptomatic (50% at time of diagnosis) – elevated Labs found on routine evaluation

Fatigue and pruritis

F/C; night sweats, RUQ pain, jaundice •

61
Q

lab values and imaging seen in Primary Sclerosing Cholangitis (PSC)

A

Labs: ↑Alk Phos, and ↑Total bilirub Cholestatic)

AST/ALT usually <300

MRCP - “beaded” appearance of the bile duct

62
Q

tx of Primary Sclerosing Cholangitis (PSC)

A

ERCP and balloon dilation/stent placement

Liver transplantation is the treatment of choice for patients with advanced liver disease

63
Q

medication options in Primary Sclerosing Cholangitis (PSC)

A
  • Cholestyramine – pruritis
  • Ursodiol (15 mg/kg) daily may be helpful for cholestasis, but not effective in prolonging survival

Steroids and immunosuppressant (Imuran, MTX

64
Q

Primary Sclerosing Cholangitis (PSC) screening

A

yearly RUQ US

or MRCP every 6-12 months, monitor CA 19-9 every 6-12 months

65
Q

lab value that is indicative of acute pancreatitis

A

Lipase >3x upper limits of normal, but will generally be >100 only cause making lipase this elevated

66
Q

lab values seen in acute pancreatitis that show:

greater risk of mortality

severity

A

BUN >20 = greater risk of mortality

CRP >150 assoc w/ severe pancreatitis

67
Q

most common causes of acute pancreatitis

A
  • Gallstones – (40-70%)
  • ETOH – (25-35%)
68
Q

si/sx of acute pancreatitis

A

Sudden onset severe epigastric pain radiating to the mid-back

nausea, vomiting

Anorexia

Tachycardia

abdominal guarding, distention

hypotension(sometimes), fevers, tachypnea

ecchymosis in the periumbilical area (Cullen’s Sign)

along the flank (Grey-Turner Sign)

69
Q

culllen and grey turner signs are seen w/ what dx?

A

Acute pancreatitis

70
Q

si/sx of chronic pancreatitis

A

Abdominal pain – epigastric and radiates to the back

Pancreatic insufficiency – fat malabsorption causing steatorrhea, malabsorption of vitamins A,D,E,K and B-12

Glucose intolerance

71
Q

risk factors for chronic pancreatitis

A
  • ETOH
  • Recurrent acute pancreatitis
72
Q

lab and imaging values in chronic pancreatitis

A

Normal Lipase – not reliable

Calcifications on US

73
Q

tx of acute pancreatitis

A

IV Fluid Replacement**: Cornerstone of management

Repeat labs assessing BUN/Creatinine, HCT q8-12 hours

Monitor CRP at 48 hours

74
Q

tx of chronic pancreatitis

A

Pancreatic enzymes - approximately 30,000 international units (IU) of lipase per meal

Fat restriction <20 g per day

Vitamin supplementation

Celiac nerve block/neurolysis – via EUS or percutaneous

Glucose management

75
Q

in acute pancreatitis Patient should have a follow-up _____ in ____ months to ensure healing and rule-out underlying pancreatic tumors

A

•Patient should have a follow-up MRCP in 2-3 months to ensure healing and rule-out underlying pancreatic tumors

76
Q

85% of pancreatic cancers are due to ____ _____ of the pancreas

A

85% of pancreatic cancers are due to ductal adenocarcinoma of the pancreas

77
Q

3rd leading cause of death from cancer in the United States

A

pancreatic cancer

78
Q

si/sx of pancreatic cancer

A

Painless jaundice

Initially asymptomatic until advanced disease

Weight loss

Pruritis

Dark urine

Pale stools , Steatorrhea

Epigastric pain

Palpable gallbladder(Courvoisier’s sign)

Glucose abnormalities (new onset diabetes)

79
Q

imaging modality for pancreatic cancer

if metastasis present?

A

Contrast-enhanced CT – pancreas protocol*

Histological diagnosis – Endoscopic Ultrasound guided core needle biopsy of pancreatic tumor, or percutaneous liver biopsy if metastasis present

80
Q

CA19-9 tumor marker is useful to identify

A

pancreatic cancer

81
Q

tx of pancreatic cancer

A

Resectable dz –modified whipple, pancreatectomy

  • Tumor in the head or uncinate process - Pylorus-sparing pancreaticoduodenectoy(modified Whipple procedure)
  • Body and tail – distal pancreatectomy

Locally Advanced Disease (30%): Radiation and Chemo – goal is to shrink tumor to a resectable size

Advanced Metastatic Disease (60%) - Systemic chemo

82
Q

major risk factors for gallstone formation

A

pregnancy

rapid weight loss

83
Q

symptomatic cholithiasis may be confused with??

A

heartburn or indigestion

84
Q

acquired diabetes and malabsorption of fat soluable vitamins make you think??

A

chronic pancreatitis

85
Q

painless jaundice makes you think??

A

biliary or pancreatic malignancy

86
Q

stages of Liver Cirrhosis

A

Compensated

Compensated w/ varices

Decompensated à Ascites, variceal bleeding, encephalopathy, jaundice

87
Q

common causes of Liver Cirrhosis

A
  • Hepatitis C (26%)
  • Alcoholic liver disease (21%)
  • Hepatitis C plus alcoholic liver disease (15%)
  • NAFLD
88
Q

major complication of Liver Cirrhosis

A

Ascites (60% within 10 yrs)

89
Q

si/sx of liver cihrrosis

A

Symptoms are with LATE STAGE disease so most have NO SYMPTOMS

Appearance of chronic illness

Palpable/firm liver (hard sharp nodular edge) -70%

Splenomegaly – 35-50%

Abdominal and thoracic superficial veins are dilated (caput medusa)

Ascites

90
Q

labs and imaging tests in liver cihrosis

A

Often absent or minimal abnormalities in early or compensated

U/S – liver size, ascites, nodular liver

FibroSure test - Predicts stage of fibrosis in HCV, ASH, NASH

Transient elastography (fibroscan) -US passes a vibratory wave through the liver and measure hepatic fibrosis or liver stiffness

91
Q

what is the MELD Score

A

MELD Score - Prognostic scoring system for end stage liver disease +/-cirrhosis 3 mo survival in patients with end stage liver disease

92
Q

tx of liver cihorrosis

A

liver transplant

93
Q

pHTN is defined as

A

Increased hydrostatic mmhg w/in portal vein >10- 12mmhg (collaterals begin to develop)

•As mmhg increases blood flow decreases and then mmhg transferred to portal vein tributaries w/ subsequent dilation = collateral formation

94
Q

Sequelae of portal HTN

A
  • Ascites
  • Esophageal and gastric varices
  • Hepatic encephalopathy
  • Splenomegaly and thrombocytopenia
95
Q

causes of pHTN

Pre-hepatic

Intra-hepatic

Post-hepatic

A

Pre-hepatic

•Portal vein thrombosis

  • Splenic vein thrombosis
  • Portal vein atresia/stenosis

Intra-hepatic

•Cirrhosis** - Etoh or chronic hepatitis

Post-hepatic

  • Budd-Chiari
  • Extrinsic tumor compression

•Right heart failure

96
Q

screening in pHTN

A

Screening EGD for varices and then annually

97
Q

tx of pHTN

A

Prophylactic treatment (reduce first variceal bleed liklihood by 50%)

  • Nonselective beta-blockers (nadolol or propranolol)
  • Reduce portal and collateral blood flow
  • Mild decrease on portal pressure
98
Q

Pathologic accumulation of excess fluid in the peritoneal cavity -> Due to hepatic and nonhepatic causes

•cirrhosis (80% cause b/c of portal HTN)

A

ascites

99
Q

si/sx of ascites

A

need abt 1500ml for PE dx so relatively inaccurate

Abdominal distension

Bulging flanks

Shifting dullness to percussion

Fluid wave

100
Q

imaging and labs in ascites

A

U/S

Paracentesis

  • SBP?
  • Cell count - w/ elevated WBC
  • Culture and gram stain
  • Glucose, LDH, protein, albumin

Albumin and total protein

101
Q

tx of ascites

A

First line – Na Restriction

Second line – diuretics (spiro / Furosemide)

Surgical

  • Large volume paracentesis – symptomatic relief
  • TIPS – relief of ascites
  • Liver transplant
102
Q

Late Cirrhosis induced MS changes (chronic cirrhosis)

•Up to 70% of patients w/ cihorrosis

A

Hepatic Encephalopathy

103
Q

si/sx of Hepatic Encephalopathy

A

Symptoms range alert w/ minor impairment memory, coordination, cognition to coma

•asterixis, twitchines

104
Q

lab and imaging findings in Hepatic Encephalopathy

A

Ammonia elevation

EEG findings high-amplitude low-frequency waves and triphasic waves

105
Q

tx of Hepatic Encephalopathy

A

Lactulose

Antibiotics (xifaxan-nonabsorbable antibiotic which absorbs ammonia)

106
Q

causes of Gastroesophageal Varices

A

Increased portal vein pressure causes varices

•Diversion of blood back to systemic veins d/t high mmhg through liver thus forming collaterals between IVC & SVC and portal venous system

107
Q

si/sx of Gastroesophageal Varices

A

Hematemesis/melena/hematochezia

Pale, hypotensive, lightheaded, syncope, orthostatic, tachycardic

Liver disease/Cirrhosis signs

AMS (encephalopathy)

108
Q

red whale sign is indicative of??

A

Gastroesophageal Varices

red marks on varices = red wale sign

109
Q

tx of gastroesophageal varicies

A

Octreotide

Abx – 3rd gen ceph

Band ligation ** - prevention of rebleed

TIPS

Angiotherapy

Liver transplant

110
Q

infectious and noninfectious causes of hepatitis

A

Infectious

  • Viral (Hep A, B, or C)
  • Fingal
  • Bacterial
  • Parasitic

Non-infectious

  • Autoimmune
  • Toxins/drugs (ex. Tylenol OD, IVDU)
  • ETOH
  • Metabolic diseases
111
Q

lab value indicative of hepatitis

A

elevated out of proportion­­­ transaminases (AST/ALT)

Hyperbilirubinemia

112
Q

ETOH Hepatitis

labs

tx?

A
  • ETOH (AST/ALT ration 2:1 not greater then 300)
  • US = ascites, fatty liver

Steroid - Methyl prednisone

Pentoxiphylline - if steroids CI

Liver transplant after 6 mo no ETOH

113
Q

hepatitis spread Fecal-oral route transmission assoc w/ crowding and poor sanitation

Lab values?

Tx?

A

Hep A

Fecal-oral route transmission assoc w/ crowding and poor sanitation

Symptomatic treatment

Clinical recovery w/in 3 mo and no chronic liver disease

114
Q

hepatitis Transmitted infected blood products, sexual contact, delivery by HBV+ mother

A

Hep B

115
Q

dx tests for Hep B

A
  • HBsAG - first evidence of infection and if persistent >6mo after illness indicates chronic infection
  • HBV DNA - active viral replication, = predictor of cirrhosis and HCC
  • Anti-HBc - – IgM indicating acute hepatitis infection and IgG indicating chronic or recovered infection
  • Anti-HBs - – after successful vaccination or recovery from HBV infection
116
Q

tx of hep B

A

Chronic

•Entecavir, Tenofovir

117
Q

Associated with extrahepatic manifestations what hepatitis?

what are these manifestations?

A

Hep B Glomerulonephritis (mostly children)

•Polyarteritis nodosa (diffuse vasculitis w/ 30% mortality w/in 5yr)

118
Q

HBV Risk factors for progression to cirrhosis, liver failure, HCC

A
  • Persistently elevated HBV DNA or ALT
  • Older, male, FHx HCC
  • AFP elevated
  • Co-infection any hepatitis
119
Q

ONLY associated w/ HBV infection and only when HBsAg present

testing?

prognosis?

A

Hep D

  • Testing = anti-HDV
  • In combination w/ chronic HBV carries worse short term prognosis w/ often rapid FHF or progression to cirrhosis
120
Q

hepatitis See typically only in immunocompromised patients

•Uncommon in US but consider if travel to endemic areas i.e. Central and SE asia, Middle east, North Africa.

A

Hep E = fecal oral transmission (waterborne)

121
Q

hep C dx tests

A
  • Anti-HCV ELISA - moderate sensitivity and specificity
  • HCV RNA – confirmatory
122
Q

tx of hep C

A

Ledipasvir/sofosbuvir -Harvoni

•Clinical recovery in 3-6 mo w/ low overall mortality <1%

Usually asymptomatic or mild clinical illness w/ 6-7 wk incubation but 85% develop chronic HCV

123
Q

hepatitis in Usually young to middle aged women

A

Autoimmune

Often insidious onset but near 40% acute hepatitis presentation can be following viral illness or drug exposure

124
Q

autoimmune hep lab values

A
  • Transaminases >1,000
  • (+) ANA
  • Elevated IgG
  • Liver bx
125
Q

tx of autoimmun hep

A
  • Corticosteroids
  • Mercaptopurine
  • +/- azathioprine
126
Q

HCV inreased risk of developing liver cihorrosis if

A
  • Chronic alcohol ingestion
  • Male
  • HCV >40yo
  • Co-infection with HIV and/or HBV
127
Q

complications fo hepatitis

A
  • Encephalopathy (­ ICP)
  • Chronic hepatitis
  • HCC
128
Q

Hepatocellular carcinoma (HCC) is caused by

A

Underlying liver dz

  • Cirrhosis
  • NASH
  • NAFLD
129
Q

labs and imaging modalities inn HCC

A
  • Labs (ex. alpha-fetoprotein)
  • US- screen for hepatic nodules in high risk pts
  • CT
  • MRI
130
Q

biospsy requirements for HCC

A

Biopsy (based on size) – diagnostic!

  • <1 CT/MRI and follow every 3 mo to assess for enlarging lesion
  • 1-2cm lesions bx should be performed
  • 2 cm, cirrhosis, characteristic imaging studies (arterial hypervascularity and delayed washout), and elevated AFP values can be managed without biopsy
131
Q

tx of HCC

A

Surgical

  • Resection
  • Liver transplant

Medical/palliative

  • Sorafenib (VEGF blocker – slows progression w/ advanced HCC
  • TACE/TARE – tx via hepatic artery ois a bridge to transplant

Chemotherapy ineffective and radioinsensitive tumor

132
Q

si/sx of hepatitis

A
  • Constitutional Sx (ex. fatigue/malaise, anorexia, N/V, fever)
  • Hepatomegaly
  • Jaundice
133
Q

AST/ALT ration 2:1 not greater then 300 is seen in ..?

A

ETOH Hepatitis

Clin Med III - GI (3 decks)

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